The overall goal of this study is to use continuous arterial spin labeling, CASL, perfusion MRI to characterize diaschisis and determine its contribution to hemiparesis after subacute stroke. Stroke remains the leading cause of death worldwide despite improvements in acute stroke treatment and prevention. Patients show considerable variability in the degree to which they recover and the mechanisms underlyingthis variabilityare still largely unknown. One mechanism, termed diaschisis, was proposed almost a century ago to explain part of the initial deficit and the ability topartially recover from it. Diaschisis refers to a reduction of cerebral blood flow in uninjured brain regions that are connected to the area of injury. Animal models suggest that the reduction in cerebral blood flow is the result of decreased neuronal activity in the connected areas. Withinthis framework, the initial deficit is due to combination of diaschisis and the loss of function at the lesion location, whereas recovery occurs as diaschisis reverses. Previous attempts to study this phenomenon in humans have relied on PET and SPECT, which are expensive, not widelyavailable, and require injection of radioactive tracers, limitingthe frequency and practicality of use. As a result, there have been relatively few studies of diaschisis and thus its relevance to stroke deficit and stroke recovery remains to be determined. Here we propose to use arterial spin labeling, ASL, to investigatediaschisis in patients in the subacute and then chronic phases after hemiparetic stroke. ASL is non-invasive MR method that quantifies blood flow. To date it has been used to measure cerebral blood flow, CBF, that has been compromised by vascular occlusive disease. Here we propose a novel application of ASL for detection of decreases in CBF due to reduction in neuronal activity. The main aim of this grant is to demonstrate reductions in CBF in the contralateral cerebellum (crossed cerebellar diaschisis)and in the contralesional hemisphere. We will then correlate these changes with initial motor deficit in 3 to 4 weeks after stroke and with degree of recovery at 6 months.